Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

At the present time, it seems unlikely that progressive neurodegenerative diseases, such as ALS, Parkinson's disease, and dementia of the Alzheimer type, are triggered by environmental agents with excitotoxic potential. These include excitotoxic agents that behave as glutamate agonists or disrupt energy metabolism: both types elicit permanent but self-limiting neuronal diseases with patterns of neuronal deficit that reflect selective chemical exposure (MPP+ and parkinsonism), differential susceptibility to energy dysmetabolism (NPA and dystonia), or the distribution of glutamate-receptors (domoic acid and memory loss). If environmental agents play an etiologic role in progressive neurodegenerative diseases, they are likely to target a critical, irreplaceable neuronal molecule that is required to maintain long-term neuronal integrity.
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PMID:Are human neurodegenerative disorders linked to environmental chemicals with excitotoxic properties? 132 79

Evaluation with the geriatric depression scale carried out in 30 patients with Parkinson's disease who did not present subjective complaint of loss of memory or impairment in superior mental function capable of interfering in daily routine showed a high frequency of depression of 50-70% depending on where the cut-off in the geriatric depression scale was located. Depression in these patients does not significantly relate with either cognitive impairment or the degree of motor incapacity. Neither were depression or anxiety in these patients related with demographic data such as the age of the patient, age at onset of the disease, sex, months of evolution, or education. In contrast, a positive correlation was found between depression and anxiety.
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PMID:[Depression in Parkinson's disease and its relation to the cognitive and motor manifestations]. 141 86

While the cause of Parkinson's disease (PD) remains unknown, recent evidence suggests that certain external factors, ie, environmental agents, may act as neurotoxins, initiating the chain of oxidative reactions that ultimately destroy neurons in the substantia nigra. Young-onset PD might result from greater exposure to a putative neurotoxin. This hypothesis has rekindled interest in the epidemiology of PD. We therefore conducted a detailed analysis of various environmental exposures and early life experiences in 80 patients with old-onset PD (at an age older than 60 years), 69 young-onset patients (younger than 40 years), and 149 age- and sex-matched control subjects. Contrary to previous reports, we were unable to implicate well water or exposure to herbicides, pesticides, or industrial toxins as significant PD risk factors. A residential history of rural living was reported by more patient cases than control subjects and was marginally significant. On the other hand, at least one episode of head trauma "severe enough to cause vertigo, dizziness, blurred or double vision, seizures or convulsions, transient memory loss, personality changes, or paralysis" occurred significantly more often prior to disease onset in patients with both young-onset and old-onset PD than in control subjects (odds ratio = 2.7). When adjusted for head trauma and rural living, smoking was inversely associated with PD, as has been previously reported (odds ratio = 0.5). There were no significant differences in early life experiences or environmental exposures between young-onset and old-onset patients. We suggest that the risk of developing PD is influenced by a variety of factors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The epidemiology of Parkinson's disease. A case-control study of young-onset and old-onset patients. 195 12

The discovery of a specific association between nerve growth factor (NGF) and basal forebrain cholinergic neurons (BFCNs) marks the beginning of a new era of research into neurodegenerative diseases such as Alzheimer disease (AD). Degeneration of BFCNs appears to be one of the earliest and most prominent neuropathological features of a broad range of diseases of the human brain that give rise to loss of memory and dementia (including, in addition to Alzheimer disease, Parkinson disease, Lewy body dementia, progressive supranuclear palsy, dementia pugilistica, olivopontocerebellar atrophy, and Wernicke-Korsakoff syndrome). Selective localization of NGF receptors on BFCN, the relatively high levels of NGF mRNA in BFCN target areas, and numerous effects of exogenous NGF in vivo and in vitro provide overwhelming evidence that the structure and function of BFCNs in the adult brain are dependent on this molecule. The question then arises as to how this special relationship is disturbed in the diseased human brain? Initial investigations in AD have already indicated a normality of NGF mRNA and retention of receptors in the basal forebrain region. Interpretation of these results and the therapeutic relevance of NGF obviously depend upon future developments in understanding the role of NGF in the normal and pathological brain.
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PMID:Nerve growth factor and the basal forebrain cholinergic system: a link in the etiopathology of neurodegenerative dementias? 218 Apr 39

Patients with dementia of the Alzheimer type (DAT) received two tests of visual selective attention, together with tests of spatial and visual recognition memory and visuospatial conditional learning previously used to show deficits early in the course of DAT. One set of attentional tests compared visual discrimination learning along intra- and extra-dimensional shifts, using a "total change" design. In the 12 DAT patients capable of attempting the extra-dimensional shift (subgroup 1), performance was equivalent to that of controls. This subgroup was also unimpaired at simple and compound discrimination learning and reversal and an intra-dimensional shift. They were as accurate as controls on a visual search task requiring matching of stimuli on two dimensions with variable numbers of alternatives, but were significantly impaired in the tests of recognition memory and learning. By contrast, the other 13 patients showed marked impairments in the attentional tasks. This subgroup was also significantly worse than subgroup 1 in performance on the visual recognition and conditional learning tasks, and showed greater severity on most of the clinical ratings of dementia. The sparing of attentional shifting in patients early in the course of DAT is contrasted with the impairments previously described in patients with Parkinson's disease with only mild or absent memory loss. The implications of this double dissociation of deficits for understanding the neural bases of the cognitive deficits in these two neurodegenerative diseases are discussed and their significance for the staging of DAT is considered.
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PMID:Sparing of attentional relative to mnemonic function in a subgroup of patients with dementia of the Alzheimer type. 229 Apr 94

Numerous pathogenetic mechanisms may lead to the progressive loss of memory and intellectual function known as dementia. Currently, the dementias are classified according to clinicopathologic entities, although for clinical diagnosis, this introduces a degree of uncertainty. Characteristic patterns of behavior and anatomic pathology have been associated with specific clinicopathologic entities. Although somewhat simplistic, classification of the dementias as cortical vs subcortical embodies the precept that brain substrate is intimately tied to behavior. Lessons in brain-behavior relationships are reviewed for four clinicopathologic entities: Alzheimer's disease, Pick's disease, vascular dementia, and Parkinson's disease. Dementing illnesses have contributed significantly to our understanding of brain-behavior relationships. Major progress can be anticipated as diagnostic issues are resolved and biological and state-specific markers emerge.
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PMID:Dementia. A review emphasizing clinicopathologic correlation and brain-behavior relationships. 266 51

Primary care physicians have a vital role to play in identifying depression in their elderly patients. Diagnosis may be difficult, because symptoms are atypical and frequently include psychomotor agitation, somatic symptoms, and complaints of memory loss. Patients with medical illnesses, such as cancer, postmyocardial infarction, stroke, Parkinson's disease, and early Alzheimer's disease are particularly vulnerable to depression. Drugs that may cause depressive symptoms are digitalis at toxic levels, beta-blockers, centrally acting antihypertensives, immunosuppressants, and nonsteroidal anti-inflammatory agents. Cyclic antidepressants are the drugs of first choice. Selection depends on the patient's physical health and current medications and the side effect profile of the drug. Side effects are more pronounced in old age because of drug accumulation owing to slowed clearance. Troublesome side effects are anticholinergic effects, orthostatic hypotension, sedation, cardiotoxicity, and weight gain. The most useful antidepressants for geriatric patients are the secondary amines, desipramine and nortriptyline. The second-generation drug trazodone has the advantage of causing the least anticholinergic effects, but it is very sedating. Before treatment, the patient should have an electrocardiogram, liver function tests, tonometry, sitting and standing blood pressures, evaluation of urinary symptoms for outflow obstruction, review of current medications, and estimation of suicide risk. Cyclic antidepressants are contraindicated during recovery from myocardial infarction, in heart disease when there is severe impairment of myocardial performance, in seizure disorders, and in the presence of glaucoma or a large prostate. Drug interactions that may cause trouble can occur with epinephrine, MAO inhibitors, thyroid hormone, cimetidine, and centrally acting antihypertensives. Dosage should start low, increasing usually by 25 mg every 4 to 5 days until a therapeutic level is reached. Failure of a noradrenergic antidepressant after 4 to 5 weeks can be followed by a trial of a serotonergic drug. Drug serum level monitoring is useful for imipramine, desipramine, and nortriptyline. Monoamine oxidase inhibitors are effective in many elderly patients who are resistant to TCAs. Sympathomimetic drugs must be avoided with MAOIs. Elderly patients are at high risk of toxicity and drug interactions with lithium. Electroconvulsive therapy is useful for patients who do not respond to drug treatment, but medical complications, particularly cardiovascular, often occur in patients 75 or older. Many patients relapse after ECT. Psychotherapy together with pharmacotherapy may be the optimal treatment for elderly depressives. Older patients are more likely to become chronically depressed than younger patients. The risk of suicide in depressed elderly males is high, particularly in those with psychosocial problems, and depression rises with age.
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PMID:Management of depression in the elderly. 266 41

The authors review the concept of subcortical dementia, specifically the dementia associated with Huntington's disease, Parkinson's disease, and progressive supranuclear palsy, all subcortical processes that involve deterioration of mental abilities. Subcortical dementia affords a unique opportunity to study the progressive memory loss associated with dementia because, in contrast to cortical dementias such as Alzheimer's disease, this relatively circumscribed syndrome does not involve dysfunction of language (aphasia) and perception (agnosia and apraxia). Research strategies are proposed to examine the concept of subcortical dementia, an entity that remains controversial and not well understood. The subcortical dementias may constitute a group of partially treatable forms of dementia.
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PMID:The concept of subcortical dementia. 293 22

Even in nonfamilial cases of dementia there is some evidence of a genetic factor. This may be linked to defective expression of neurofilament protein and also abnormal phosphorylation of cytoskeletal proteins. In this respect there may be a link with accumulation of tangles and amyloid which have some degree of homology. It may be speculated that neurons containing tangles or undergoing granulovacuolar degeneration would not be able to release trophic factors and that transneuronal degeneration would result. However, the environmental or aetiological factors associated with Alzheimer's disease are not known. Although there has been a failure to transmit Alzheimer's disease to primates, it is possible that as in postencephalitic Parkinson's disease virus may be implicated at some stage in the pathogenesis. Finally, free radical formation has been considered as an alternative mechanism for death of large neurons within the CNS. Although tangles are found in several other dementing conditions (e.g. dementia puglistica, Parkinson-dementia complex of Guam), Alzheimer-type plaques and tangles are not invariably found in cases of cognitive deficit. For example, in dementia of Parkinson's disease there is a low neuritic plaque count and normal population of tangles. In addition, memory loss is not necessarily associated with defects in the cholinergic system and/or loss of nucleus basalis nerve cells. We have proposed that damage to or loss of cortical cells may be a more general finding in dementing illness.
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PMID:Pathophysiology of ageing brain. 330 42

Sixty patients with Parkinson's disease were administered a battery of neuropsychological tests. Using regression data from a matched normal control sample, age- and education-residualized test scores were obtained for the patients. Three clusters of patients were identified: those with both verbal memory and visuospatial reasoning disorders (n = 24), those with memory impairment only (n = 17) and those with normal intellectual function (n = 12). Analysis of variance and planned comparisons (Newman-Keuls) were performed to detect group differences. No difference on 9 memory measures were found between the 2 memory-impaired groups. However, these groups differed significantly on all memory measures from the group with normal function. The 2 memory-impaired groups also differed significantly from each other on all 7 measures of visuospatial reasoning. The group with memory loss only was significantly younger than the group with both visuospatial and memory impairment and also demonstrated less bradykinesia. Otherwise, there were no group differences in the severity of motor signs, disease duration or duration of levodopa therapy. These findings support a different etiology for motor and intellectual deficits in Parkinson's disease.
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PMID:Subtypes of Parkinson's disease defined by intellectual impairment. 347 20


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